Published Online
on January 25, 2007

A more recent version of this article appeared on March 1, 2007

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Submitted on September 28, 2006
Accepted on October 12, 2006

Infection After Acute Ischemic Stroke. A Manifestation of Brain-Induced Immunodepression

Ángel Chamorro MD, PhD^*; Xabier Urra MD; and Anna M. Planas PhD

From the Stroke Unit (A.C., X.U.), Hospital Clínic and Institut d’ Investigacions Biomédiques August Pi i Sunyer (IDIBAPS). University of Barcelona, Spain; and the Pharmacology and Toxicology Department (A.M.P.), Consejo Superior de Investigaciones Científicas (IIBB-CSIC) and IDIBAPS, Barcelona, Spain.

^* To whom correspondence should be addressed. E-mail: achamorro{at}ub.edu.

Background and Purpose--Infection after experimental focal ischemia may result from brain-induced immunodepression, but it is unsettled whether a similar syndrome occurs in human stroke.

Summary of Review--Many patients develop infections shortly after acute stroke regardless of optimal management. Mortality is higher in these patients and the severity of stroke is the strongest determinant of the infectious risk. However, it is controversial whether infections promote neurological worsening or alternatively represent a marker of severe disease. The brain and the immune system are functionally linked through neural and humoral pathways, and decreased immune competence with higher incidence of infections has been demonstrated in several acute neurological conditions. In experimental brain ischemia, infections are associated with the activation of the autonomous nervous system and neuroendocrine pathways, which increase the strength of anti-inflammatory signals. A strong cytokine-mediated anti-inflammatory response was recently observed in stroke patients at higher risk of infection, although infection could not demonstrate an independent association with the progression of the symptoms.

Conclusions--The appearance of infection in patients with acute stroke obeys in part to immunological mechanisms triggered by acute brain injury. An excessive anti-inflammatory response is a key facilitating factor for the development of infection, and it is likely that this immunological response represents an adaptive mechanism to brain ischemia. Contrarily, it is unclear whether infection contributes independently to poor outcome in human stroke. Overall, a better understanding of the cross-talk between the brain and the immune system might lead to more effective therapies in patients with acute stroke.

Key words: acute stroke • complications • immunology • infectious disease • pathogenesis

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